Macroautophagy (herein referred to as autophagy) is an evolutionarily conserved process by which cells utilize double-membraned autophagosomes to recruit dysfunctional components for their bulk degradation in lysosomes and ultimate recycling [1]. Autophagy plays an important role in cellular homeostasis; therefore, the dysregulation of autophagy contributes to many diseases, including cancer [2-4]. Autophagy can function as a tumor promoter to induce tumor growth, progression and resistance to microenvironmental stresses, such as starvation, hypoxia and epithelial-to-mesenchymal transition [2]. Moreover, abundant evidence has emerged to show that autophagy inhibition synergizes with chemotherapy to trigger tumor cell death [5-7]. Chloroquine (CQ) and its derivative hydroxychloroquine (HCQ), which are clinically used antimalarial drugs, also inhibit autophagy by preventing the acidification of the lysosomal compartment [8]. CQ and HCQ have recently been administered independently or in combination with anticancer drugs in clinical trials for certain types of cancers [7]. Moreover, some data show that HCQ may aid cancer treatments [9]. Nevertheless, the chemosensitizing effects of CQ/HCQ may be autophagy independent and attributable to the destabilization of lysosomes [10] and tumor vasculature [11]. Thus, drugs that target autophagy-related (ATG) proteins could provide the opportunity to test the role of autophagy in tumor malignancy.